Recent findings have shown that neonatal animals are particularly susceptible to laryngeal stimuli. The prolonged and sometimes fatal apnea that can be produced suggests that the susceptibility to sensory input from upper respiratory tract areas on respiratory neurones may have significance in the sudden infant death syndrome (SIDS). We propose to extend our survey of experimental upper airway stimuli (neural, chemical and mechanical) that elicit respiratory reflexes, particularly apnea, and study their effects on respiration, on caudal brain stem neurones concerned with repsiration, and on primary afferents recorded in the cat and kitten. The extent to which respiratory reflexes such as apnea may be modified by altering laryngeal receptors will also be studied. The observed patterns of response will be correlated with maturation of the animal with a view to gaining insight into the mechanisms underlying the age dependence of the response. In addition , we will study the effects of previous respiratory infections, such as feline rhinotracheitis, on apnea induced by upper respiratory tract stimulation because a large proportin of SIDS victims have a previous case history of respiratory tract infection. Since laryngospasm may be a possible terminal event in SIDS, mechanisms regulating the activity of the laryngeal motoneurones recorded in nucleus ambiguous and the recurrent laryngeal nerve in the infant animal will also be studied for comparison with those presently under study in the adult.